title: Non-canonical β-catenin degradation mediates reactive oxygen species-induced epidermal cell death.
abstract: β-Catenin is constantly degraded through the ubiquitin-proteasomal pathway. In this study, we report that a different type of β-catenin degradation is causally involved in epidermal cell death. We observed that reactive oxygen species (ROS) caused β-catenin degradation in the epidermal cells through a caspase-dependent mechanism, which results in disruption of cell adhesion. Disruption of cell adhesion increased ROS and activated caspases. Upregulation of the intact β-catenin blocked ROS accumulation and caspase activation. These results indicate that a feed-forward loop consisting of ROS, caspases activation and β-catenin degradation induces epidermal cell death.
authors.affiliation: Department of Environmental and Molecular Toxicology, North Carolina State University, Raleigh, NC 27695, USA.
authors.forename: E
authors.initials: E
authors.lastname: Omori
authors.forename: K
authors.initials: K
authors.lastname: Matsumoto
authors.forename: J
authors.initials: J
authors.lastname: Ninomiya-Tsuji
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000187:drug effects*; D020169:Caspases / Q000378:metabolism; D002448:Cell Adhesion / Q000187:drug effects; D004789:Enzyme Activation / Q000187:drug effects; D000078404:Epidermal Cells; D004817:Epidermis / Q000187:drug effects* / Q000201:enzymology / Q000378:metabolism; D057809:HEK293 Cells; D006801:Humans; D051379:Mice; D017382:Reactive Oxygen Species / Q000494:pharmacology*; D051176:beta Catenin / Q000378:metabolism*
chemical_list: D017382:Reactive Oxygen Species; D051176:beta Catenin; D020169:Caspases